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Since all circadian gene-mutant mouse models show increased sensitivity to γ-radiation, we conclude that the molecular clock functions in tumor suppression in vivo.
Astrocytes from DS fetal brain tissue and DS mouse models show increased concentration of intracellular calcium [55], [56], altered sensitivity to oxidative stress [57], deficits in mitochondrial energy metabolism [22], [58] and abnormal APP transport and secretion [22].
Vitamin D receptor animal knock-out models show increased anxiety, decreased activity, and muscular and motor impairments, resembling phenotypic models of depression.
Interestingly, recent studied in VAP (P56S) transgenic mice models show increased nuclear levels of ATF4 and CHOP (Aliaga et al., 2013).
All three mouse models show increased calcium release in response to IP3, relative to wild type mice [ 6, 8, 10], with results from SCA2 and SCA3 suggesting a mechanism involving supersensitive IP3R1 [ 6, 10, 18].
Furthermore, these mouse models show increased susceptibility to induced ventricular tachycardia (VT) and sudden cardiac death (SCD), supporting the belief that LQT in RTT underlies sudden death (McCauley et al., 2011).
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OA cartilage in both humans and mouse models shows increased expression of HIF-2α.
Similar observations were made in vivo in other models showing increased median survival of mice treated by everolimus first line compared with sunitinib (Rosa et al, 2013).
These data found further confirmation in two other HD mouse models showing increased striatal BimEL in R6/1 mice at the late stages of disease and in the conditional model Tet/HD94.
All models showed increased risks during the end of July and start of August, the period when the temperature had been at an extremely high level for about two weeks.
Studies in HD mouse models showed increased Bax levels in the brain mitochondrial fractions from R6/1 and R6/2 mice and increased Bax mRNA in the cortex and cerebellum from R6/1 mice, brain areas in which Bax mRNA correlated with the number of apoptotic nuclei.
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